Great. Thank you again, Charles. Good morning to everybody, and thanks for always making this so easy, and getting us going. This morning, on the second day of the Oppenheimer Healthcare Conference for our track, we've got Garo Armen, the CEO of Agenus, kicking things off. He and I were just talking about how far oncology has come and how much Agenus has been a participant in the growth, especially of knowledge around immuno-oncology, and the company's poised, looks like, to, you know, also becoming commercial sooner rather than later. So Garo, maybe if you can give us a 3-5-minute intro, and then we'll go through our fireside chat. Thank you very much, Hartaj, and thank you, everybody, for being here. As you remarked earlier, the company was founded by me and a scientific founder 30 years ago. And in fact, this year is our 30th anniversary. And at the time we started our operations, the purpose of the company was that the immune system we were convinced, as a group at that time, and we are very much convinced today, that the immune system was the Holy Grail to curing cancer. And of course, in the beginning, there were limited reagents and tools and capacities to be able to do this. But 30 years later, I think the company has in a position where we have a full armamentarium of the symphony of the immune system. And now, basically, we can pull and push different components, which we're doing in the context of our clinical trials, to do this. And the transformation started in 2014, where we bought a company, it was a private company in Europe called 4-Antibody. It was a spin-out of the Roche Research Institute in Basel, Switzerland. And that acquisition allowed us to have an antibody discovery platform, which transformed Agenus from just being a cancer vaccine company, which was a very powerful vaccine platform and still resides with us, and an adjuvant company. And that is our QS-21 adjuvant, which is the key driver of vaccines such as Shingrix, for example. Shingrix is a well over $4 billion product today. And, our cancer adjuvant, I'm sorry, our vaccine adjuvant, QS-21 Stimulon is a big driver of this. So now, after that transformation, we have brought to the clinic approximately 15 different agents, including cell therapies. And of those 15 agents, half of them have been licensed out to companies like Gilead, Incyte, Merck, Bristol-Myers, and so on, for a total consideration of over $850 million. This is not bio dollars. This is real dollars that have come into the company, to be followed, potentially, by milestones and royalties upon further development and commercialization of these products. But the other half of the portfolio is unencumbered. And one of the very exciting agents in that other half of the portfolio, which is our lead compound right now, is botensilimab, which we call a multifunctional immune activator. And the reason we call it multifunctional is because sometimes people mistakenly look at it as another CTLA-4 antibody. Of course, it binds to CTLA-4, but it does so many other things that I'm happy to explain that makes this antibody a highly versatile antibody that turns cold tumors into hot tumors. So that's where we are right now. And we can discuss the details as you unfold the questions. Absolutely, Garo. You know, it's fascinating. There's so many different ways that we can go here. Personally, I'm looking forward to, you know, continuing the conversation with you because there's just so much history, right, in drug development. You can learn from that. But, you know, let's focus on a couple of specific things here. You touched on a few things here, Garo, that I think are important. One is maybe we can just talk about the specific elements of the IO system that you're modulating with BOT and BAL, right? If you can just talk about those two antibodies and what are the specific elements of the IO, of the immune system that you're modulating, then we can take the next step, you know, with our audience, which is specialists and generalists combined, to help them out. You know, we'll talk about the data and then maybe, you know, go from there as to what are some of the, you know, regulatory and clinical next steps. So, very good point, Hartaj. Like anything else, of course, any new innovation in the cancer space comes with its challenges. And I'll explain what I mean by that. So as you remarked earlier before we start the session, for many, many years, we've been on the trail to try to do something meaningful, and that only meaningful thing could be a cure for cancer patients. And if you look at the history of cancer and drugs, first, we need to reset and try to understand what cancer is. One thing we know about cancer is that it is an individualized disease. In other words, it is different in every single patient. There's no ambiguity about that. It's genomically a different disease in every patient. And so if you look at that aspect of it, and if you look at the aspect that it is a systemic disease, even though you identify the primary root tumor often and characterize it, but the cancer spreads, and it goes to different parts of the body. So it becomes very challenging. To treat a disease like this with a drug like chemotherapy means you are trying to now, basically do something about rapidly dividing cancer cells. Of course, there are other rapidly dividing cancers in the body, including immune cells, you know, hair follicles, skin cells, and so on. So it becomes a very challenging undertaking to be able to specifically target cancer. And what you're counting on, it is our belief, is that while you are weakening cancer somewhat preferentially with chemotherapy, it's really the immune system that is doing the mopping up of the cells and cleaning it up. For example, in early-stage cancer, when you treat the patient with a chemotherapeutic, the chemotherapeutic may be sufficient to sort of get rid of a lot of the cancer cells and let the immune system do the rest. Now, of course, we don't consciously realize what's going on, but in essence, this is what's happening. Now, as the cancer progresses to late-stage disease, it becomes more and more challenging to get the job done with this very fine balance of the immune system versus the cancer or the disease. What we're doing here is specifically addressing that with an agent like BOT and BAL because one activates the cells, and the other one basically takes down the protection of the cancer. PD-1s take down the protection of the cancer, whereas a CTLA-4 binding antibody, among doing other things, activates T cells. Now, of course, doing this is rather simple in what we call hot tumors. Hot tumors are dealt with a grand total of over $50 billion worth of annual sales today, primarily driven by PD-1s and PD-L1s. But that's a small segment of the cancer pie. The big segment of the cancer pie is cold tumors. That has been insurmountable with immuno-oncology drugs until we demonstrated in the clinic in well over 750 patients across 9 different tumor types that indeed, for the first time, to the best of our knowledge, we are seeing activity with cold tumors, such as, for example, MSS-CRC. That's MSS colorectal cancer that accounts for over 90% of metastatic colorectal cancer patients. So it's a huge segment of the market. And unfortunately, today, the agents available, including chemotherapy and targeted agents, are very problematic, both in terms of toxicity as well as lasting benefit to patients. So do they help? Yes, marginally, they do provide help. But beyond that, these patients are not being either cured or seeing a benefit for years or beyond that. And what we're seeing with BOT and of course, we're in the clinic. We are accumulating the data right now. We hope to convince the Food and Drug Administration to make sure that they are on board with this. That will happen sometime around mid-year. Beyond that, we hope that we will get the clearance from them to be able to file our BLA. It will be the first BLA for BOT with colorectal cancer first, MSS colorectal, to be followed by pursuit of other cancers, such as pancreatic cancer. Garo, you know, that's really fascinating. You know, and love the way, you know, you're weaving the thread here because that makes my job easier in terms of asking the questions. You know, you're talking about now, you know, colorectal cancer. And colorectal cancer, you know, historically, I believe, has, you know, been difficult for, for example, checkpoint inhibitors to crack, right? And you've got a combination approach. You talked about hot and cold tumors. Can we just dive a little bit more before talking about the actual data that we've seen that you've generated in colorectal cancer that you'll present to the FDA? Maybe just talk a little bit about MSS high colorectal cancer. I know you talked about cold and hot tumors, but why has that been so difficult, you know, specifically for a lot of the current therapies, and some of the IO therapies that have done well to sort of crack, you know, for lack of a better term? So when we talk about cold and hot, let's first think about what does this mean, what does cold and hot mean? Well, a hot tumor is immunologically visible to things like T cells. And because they're immunologically visible, in other words, they're antennas, they're antigens on the surface of the cell, are rampant. And they're basically telling the immune system, here I am, come and get me if you can, OK? Whereas with cold tumors, these signals are not nearly as visible. And so it makes it challenging for the established immuno-oncology agents, PD-1s, PD-L1s, including the first-generation CTLA-4 agents like Yervoy and tremelimumab, it makes it difficult for them to tackle this problem. Now, the question is, when you have a cold tumor like MSS CRC, MSS, by the way, means microsatellite stable as opposed to microsatellite unstable. That's MSI-H, which accounts, as I said, for less than 10% of the late-stage tumors in CRC. So when you look at a CRC tumor that is in the category of MSS, what can we do? Well, because of the specific attributes of botensilimab, which, as I said earlier, is not a newer version of a CTLA-4 antibody, it's that plus a lot more. That plus a lot more because its Fc domain of the antibody, which is the tail of the antibody, has been completely re-engineered. And completely re-engineered for what purpose? Well, one purpose is that it attracts myeloid cells. Myeloid cells are a very important component of the immune system. I'm talking about things like macrophages, dendritic cells, and so on. And these cells tend to chew up the regional problem. And in this particular case, it would be MSS-CRC. As they chew up the regional problem, it brings the signals to the attention of the immune system. So that's one way it activates the immune system to target a microsatellite stable or what is otherwise known as a cold tumor. By the way, we're seeing similar trends in other cold tumors, such as ovarian, such as pancreatic, such as sarcomas. A good chunk of the sarcomas are known to be very cold tumors. The colder the tumor, not just a cold tumor does not respond to an immunological agent, but it has a difficult time responding to other agents, including chemotherapy. So their response to chemotherapy and target therapy is below par, so to speak. And so when we use botensilimab in combination with balstilimab, our PD-1 antibody, what it does is really convert this cold tumor into a hot tumor and then let the immune system, with a much more profound activation, do the rest of the job. Of course, botensilimab does other things. It activates T cells even better. It induces memory response, which is critically important. It downregulates regulatory T cells, which is also critically important. So it does all of these things in the context of a single molecule and hence the observation of this differential activity that we're seeing, which, by the way, the molecule was specifically designed to do all of this. And we were very encouraged to see this in preclinical experiments, exactly as I described it. And then it translated to the clinic. And as I said, not just in one cold tumor, but multiple cold tumors. Also, very importantly, Hartaj, sometimes you have hot tumors, or knowingly hot tumors, that fail conventional immunotherapy. And what we're seeing with botensilimab and balstilimab is that those patients, whether they're melanoma patients, lung cancer patients, or others that fail conventional immunotherapies, they are responding to BOT/BAL. And that's very encouraging, particularly in the context of cancer patients. Now, one other thing that I should mention is that while this is going on, clearly, we are not able to have every single patient respond. But what's encouraging is that depending on the indication that we've tested and depending on the denominator of the patients enrolled, somewhere between 20%-60% of patients are responding, as I said, depending on the indication and the denominator. Very encouragingly, you know, as you know, response rate is characterized as tumor shrinkage, which is greater than 30% versus the baseline, OK? So 30%, that's the hurdle. Now, a very substantial proportion of our patients are also between that 0% and 30%. So while they haven't been characterized as formal responders, we're seeing that in that range, 0% to 30%, these patients are in that zone for a prolonged period of time. And that's very encouraging because sometimes you can have patients that are so-called stable disease responders. And these patients will have stable disease for years. You know, de facto, that translates to them living with their disease for an extended period of time. And that's a big benefit as well. It's almost like achieving a ceasefire with the cancer, you know, I'm sure for cancer patients, they will take that if that's what they get. Garo, maybe can you just talk a little bit about the specific data that you've generated in MSS mCRC, and the data sets that you will be presenting to the FDA for that, you know, by the middle part of the year for your potential approval? Certainly. So as you know, in the last 18 months, Hartaj, we've had the privilege of presenting data at seven major conferences. These include ASCO-GI, ESMO, ESMO-GI. It includes SITC. And some of these conferences we presented several times as the data has matured. And the data that we presented, the last set of data that we presented at MSS-CRC, is based on the fact that we are seeing approximately 25% overall response rates in MSS-CRC patients who have no liver mets. Now, we have segmented out no liver met patients. And certainly, these patients are somewhat better prognosis patients, because liver mets, particularly in colorectal cancer, has a more dire outcome. But they represent a significant proportion, meaning they represent about a third of the patients and for which established therapies don't seem to result in a much better outcome than in liver patients. And so when we segment that out, the best literature and presentation data that we have seen in non-liver met patients with standard of care is response rates that are in the mid-single digits. And it is those patients that not only are we seeing response rates of around 25%, but we're seeing prolongation of these responses. So for example, the first patient treated was a patient of our Chief Medical Officer, Dr. Steven O'Day, who, before he came to join Agenus and in fact, one of the reasons, as he'll tell you, he joined Agenus is because he saw firsthand what was going on with his patients. And he was very encouraged with the data. And his thought was, yes, I can have a few patients help in my practice. But if I join the company, perhaps I can participate in the development of this drug and help masses, significant numbers of patients. And that's what he did. And we're delighted to have him on board, of course. But his very first patient, who was an elderly lady with MSS colon cancer. And she's alive and well over three years now. And so that's a big deal for the patient. And of course, statistics are important, very important, because they allow us to gauge the validity of the data, integrity of the data. But on an individual basis, it's critically important to consider that if a patient who would have died otherwise is alive and well and normally functioning at beyond three years, and we have other patients that are approaching three years now, that's very gratifying for us as a company. Of course, it's very gratifying for the physician. No, absolutely, Garo. I mean, you know, I agree with you. I mean, my own personal opinion is that, you know, the fight of cancer is going to be literally—my dad was an infantryman in the infantry in India. Sikhs mostly come from the military. He was a fifth-generation military officer. And I would have been in the military too if I'd—I was born, brought up in India. And if I'd lived there, you know, I think it's a knife fight. It's going to be a knife fight one-on-one for a very long period of time before we—I don't know if we ever get it under control, but we just can kind of delay, you know, the—I guess. But you know, so it's really impressive what all you have done. You know, if I was to ask the question another way in terms of what you're doing with the FDA, what would be probably the biggest areas of concerns for you, you know, your Chief Scientific Officer, your Medical Officer, in terms of the application? Like, are there aspects of the data that are still maybe I would call an unknown that maybe, you know, no application averages 100%, right, the probability of it getting approved? But are there parts of the data that maybe, you know, you think, you could look into more or still a little bit more of an unknown in terms of this application? Well, I mean, you are always, of course, questioning internally and externally. And this is the process that we go through. We're blessed by having some wonderful experts in the field who have direct experience with the agency. So they know what the issues may be in the minds of the regulators. And so they're helping us with that. And so far, we haven't identified you know, you asked the question, what are the typical concerns? Well, you know, remember, we're going for accelerated approval. So an accelerated approval is based on the fact that you think you have very compelling data, which we believe we have. You think that there is a major unmet need. We think we have that here, of course. And you also need to make sure that the data integrity, data quality is of the highest level. We believe we have that, by the way. Of course, it is a process that you go through. This is not just, you know, opening up a book and seeing that everything looks good in terms of numbers. It's a process of validation of the data, peeling the layers, you know, one by one, and making sure that what we have been presented by sites is indeed accurate. We go through all of that process. That's one of the reasons that we have opted to go about this strategy of accelerated approval, because of the fact that these are patients that desperately need something above and beyond the typical target therapies and chemotherapies that are available, which, by the way, are not great in terms of quality of life, also not great in terms of any really long-term benefit to patients. So because of that, we're going with this strategy. Now, given the fact that it is an accelerated approval pathway, it is laden with all kinds of challenges, of course. And this is what we hope that we will resolve with high integrity, going to the agency sometime around mid-year and showing everything that we have, just as, you know, we don't want to do this in pieces. We want to make sure that we have everything, presentable in a way that the agency will appreciate and understand. And we hope to get the OK from them that we are eligible for accelerated approval. And if we get that OK, we plan on filing sometime in the second half of this year. And that is the best outcome we expect for patients, particularly. Yep, that makes a lot of sense. I mean, that recapitulates you know a lot of companies that we talked to are going through an accelerated approval pathway, are kind of you know they say things similar to what you're saying. So that gives us you know, that helps us also as analysts. I've got about 2-3 questions on the internet. So you know we've got about 3 or 4 minutes left. So we'll do like a final Jeopardy! Garo here. First question is, when can we expect the start of the confirmatory phase 3 MSS-CRC trial? Will FDA accept the BLA for accelerated approval without the confirmatory trial, you know, into enrollment? So is there a risk if the phase 3 has not been activated yet? No, I think that what will happen is that when we go to the FDA first of all, the FDA had given us their blessings on a randomized phase three trial plan, last year. So we have that. But since then, some of the standards of care have changed. So but while the basic trial design is intact, we believe that the changes in standard of care, for example, regorafenib plus Avastin now is becoming more of the standard of care. And, so we need to have a control arm, a reference arm that will take that into consideration. But we hope that all of these will be presented to the agency and resolved at the time of our, sort of, end of phase two, meeting, if you will. and that at that point, we are basically teeing up to make sure that we can pull the trigger and initiate the trial immediately. Now, we are fairly confident, Hartaj, that the trial will enroll quickly for 2 reasons. One, when we did the phase 2 randomized trial initiation, we enrolled nearly 250 patients in less than 4 months. That was a record time frame for enrollment. And the reason we enrolled is because of the enthusiasm of the practitioners, the KOLs, the investigators out there, that they are really looking forward to the treatment of their patients with our agents. And so we believe that in the context of phase 3, the enrollment will be also very rapid. So as of now, we don't anticipate this will be a stumbling block. Not a gating factor. Great. A couple more questions, Garo. When to expect the BLA and what indications? I think you had already mentioned this, but just if you don't mind going through it. The first indication will be MSS-CRC in non-liver met patients. These are second- and third-line patients. We already have a fast track allowance from the FDA with a read that almost reads like the label of the product. This is a readily identifiable patient population, as per our consultations with all the experts in the field. Because of the dire need for these patients, they are looking forward to enrolling patients in their practice. Yep. And then last question, Garo, is, do you plan on filing the BLA in the EU for BOT/BAL? Well, as of now, the plan is for accelerated approval filing in the U.S. only. EU requirements are somewhat different. We are engaged with the EU authorities right now. And we will continue to engage with them. But my expectation is that, should we succeed with the accelerated approval pathway in the U.S., EU filing will probably follow within the following 12 months or so. Garo, a real pleasure. We could have gone on for another half an hour, 60 minutes. I'm pretty sure it's amazing the amount of knowledge you have and what you're able to encapsulate in this short time. So we really appreciate it. We look forward to keeping the conversation going. Thank you, Hartaj. Thank you, Oppenheimer, for allowing us this opportunity.